Vitamin D as prevention of osteoporosis may be inappropriate

The common practice of administering vitamin D supplementation for the prevention of osteoporosis among adults may be unnecessary, according to data reported in The Lancet.

“The negative findings of our analysis contrast with the widely held perception that vitamin D works directly on bone cells to promote mineralization,” Ian R. Reid, MD, of the University of Auckland in New Zealand, and colleagues wrote. “The increasing practice for measurement and supplementation of vitamin D is expensive. Our data suggest that the targeting of low-dose vitamin D supplements only to individuals who are likely to be deficient could free up substantial resources that could be better used elsewhere in health care.”

Ian R. Reid, MD 

Ian R. Reid

Various databases were searched for trials examining the effects of vitamin D (D3 or D2, but not vitamin D metabolites) on bone mineral density. The primary endpoint was the percentage change in BMD from baseline, according to data. Ultimately, the researchers identified 23 studies (mean duration, 23.5 months) that included 4,082 patients (92% women; mean age, 59 years).

The mean baseline serum 25-hydroxyvitamin D concentration was <50 nmol/L in eight of the studies (n=1,791) examined by Reid and colleagues. They also found that patients were given vitamin D doses <800 IU daily in 10 studies (n=2,294). Patients’ BMD was measured in each study at one of the following sites: lumbar spine, femoral neck, total hip, trochanter, total body or forearm, according to data.

The researchers reported that six studies showed significant benefits to BMD, four reported beneficial effects at one site only, and one reported beneficial effects in both femoral regions. The other sites in each study did not show benefit from treatment and two studies reported detrimental effects at the total body (P≤.05).

Researchers found a small benefit at the femoral neck (0.8%; 95% CI, 0.2-1.4) with heterogeneity among trials, according to abstract data.

“Although small increases in bone density at some skeletal sites in some studies were reported, when these increases are offset against the individual findings of deleterious effects, the number of positive results is little better than what would have been expected by chance,” the researchers wrote.

Clifford J. Rosen, MD 

Clifford J. Rosen

In an accompanying editorial, Clifford J. Rosen, MD, director of clinical and translational research and a senior scientist at Maine Medical Center’s Research Institute, wrote that Reid and colleagues’ analysis is consistent with the current understanding of vitamin D; that its supplementation is not needed to prevent osteoporosis.

“However, maintenance of vitamin D stores in the elderly combined with sufficient dietary calcium intake (800 mg to 1,200 mg per day) remains an effective approach for prevention of hip fractures,” Rosen wrote.

For more information:

Reid IR. Lancet. 2013;doi:10.1016/S0140-6736(13)61647-5.

Rosen CJ. Lancet. 2013;doi:10.1016/S0140-6736(13)61721-3.

Disclosure: The researchers report no relevant financial disclosures. Rosen reports no disclosures.

The common practice of administering vitamin D supplementation for the prevention of osteoporosis among adults may be unnecessary, according to data reported in The Lancet.

“The negative findings of our analysis contrast with the widely held perception that vitamin D works directly on bone cells to promote mineralization,” Ian R. Reid, MD, of the University of Auckland in New Zealand, and colleagues wrote. “The increasing practice for measurement and supplementation of vitamin D is expensive. Our data suggest that the targeting of low-dose vitamin D supplements only to individuals who are likely to be deficient could free up substantial resources that could be better used elsewhere in health care.”

Ian R. Reid, MD 

Ian R. Reid

Various databases were searched for trials examining the effects of vitamin D (D3 or D2, but not vitamin D metabolites) on bone mineral density. The primary endpoint was the percentage change in BMD from baseline, according to data. Ultimately, the researchers identified 23 studies (mean duration, 23.5 months) that included 4,082 patients (92% women; mean age, 59 years).

The mean baseline serum 25-hydroxyvitamin D concentration was <50 nmol/L in eight of the studies (n=1,791) examined by Reid and colleagues. They also found that patients were given vitamin D doses <800 IU daily in 10 studies (n=2,294). Patients’ BMD was measured in each study at one of the following sites: lumbar spine, femoral neck, total hip, trochanter, total body or forearm, according to data.

The researchers reported that six studies showed significant benefits to BMD, four reported beneficial effects at one site only, and one reported beneficial effects in both femoral regions. The other sites in each study did not show benefit from treatment and two studies reported detrimental effects at the total body (P≤.05).

Researchers found a small benefit at the femoral neck (0.8%; 95% CI, 0.2-1.4) with heterogeneity among trials, according to abstract data.

“Although small increases in bone density at some skeletal sites in some studies were reported, when these increases are offset against the individual findings of deleterious effects, the number of positive results is little better than what would have been expected by chance,” the researchers wrote.

Clifford J. Rosen, MD 

Clifford J. Rosen

In an accompanying editorial, Clifford J. Rosen, MD, director of clinical and translational research and a senior scientist at Maine Medical Center’s Research Institute, wrote that Reid and colleagues’ analysis is consistent with the current understanding of vitamin D; that its supplementation is not needed to prevent osteoporosis.

“However, maintenance of vitamin D stores in the elderly combined with sufficient dietary calcium intake (800 mg to 1,200 mg per day) remains an effective approach for prevention of hip fractures,” Rosen wrote.

For more information:

Reid IR. Lancet. 2013;doi:10.1016/S0140-6736(13)61647-5.

Rosen CJ. Lancet. 2013;doi:10.1016/S0140-6736(13)61721-3.

Disclosure: The researchers report no relevant financial disclosures. Rosen reports no disclosures.